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Spring 2016 - CVPR > CV_2 > Flashcards

CV_2 Flashcards

1
Q

Oxygen delivery to heart equation

A

Oxygen delivery = coronary blood flow* oxygen content

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2
Q

What are 5 ways smoking confers a 50% increase in cardiovascular disease risk?

A
  1. Thrombogenic
  2. Compounds prmote atherosclerosis
  3. Endothelial dysfunction/vasospasm
  4. CO decreases oxygen delivery
  5. Decreased HDL
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3
Q

What is the dyslipidemic triad?

A

High LDL
Low HDL
High triglycerides
They are independent risk factors

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4
Q

When heart rate increases, what part of the heart contraction cycle shortens?

A

Diastole. Thus, tachycardia can compromise coronary flow

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5
Q

How do you increase myocardial O2 supply?

A

Increase blood flow, since the heart can’t increase oxygen extraction

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6
Q

What is the Law of Laplace?

A

Myocardial wall tension is proportional to cavity pressure, cavity dimension, and 1/ wall thickness

T oc P*L/WT

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7
Q

Acute myocardial infarction is also called ___________

A

Unstable angina

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8
Q

What are the 2 most common vessels used for coronary bypass surgery?

A

Mammary artery

Saphenous vein

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9
Q

What is the primary component of large arteries, small arteries, and arterioles?

A

Elastin
Collagen
Smooth muscle

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10
Q

Can LDL enter the endothelium?

A

Not under normal conditions. It can only enter disrupted/abnormal endothelium

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11
Q

What is the composition of venous and arterial thrombi? Where do they occur? What drug classes are used to treat?

A

Venous: fibrin and RBC-rich. Occur in areas of stasis. Treat with anticoagulants.
Arterial: platelet-rich. Occur in areas of high flow. Treat with antiplatelets.

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12
Q

What measureable thing is elevated in myocyte necrosis?

A

Troponin enzymes (I and T)

Begin 3-12 hours after injury and peak 18-24 hours after necrosis begins

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13
Q

What does LDL bind to in the intima, resulting in entrapment?

A

ECM proteoglycans

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14
Q

What is the pathophysiological difference between STEMI, NSTEMI, and unstable angina??

A

STEMI - complete coronary vessel occlusion

NSTEMI - partial coronary vessel occlusion with myocardial necrosis

Unstable angina - partial coronary vessel occlusion without myocardial necrosis

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15
Q

Draw the serum markers of myocardial necrosis chart

A

Mrr

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16
Q

What is the difference between stable and unstable angina?

A

Unstable is when angina symptoms change and are worse

Unstable is on the spectrum of acute coronary syndrome and stable angina is not

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17
Q

What are the 2 ways to reduce artery occlusion in STEMI (complete coronary artery occlusion)?

A

Cardiac catheterization

Fibrinolytics - if can’t be opened within 90 minutes or cath lab is not available

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18
Q

What is coronary autoregularion?

A

When coronary blood flow responds to coronary artery pressure to keep it at a certain level. So, when pressure increases, blood vessels relax and stuff.

Occurs at level of small arterioles

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19
Q

How well does angiography estimate the size and severity of coronary artery disease?

A

It usually underestimates it because it can only observe lumenal diameter.

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20
Q

What are 5 upregulators of nitric oxide?

A 
Shear stress
Acetylcholine
Serotonin
Thrombin
Bradykinin
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21
Q

What are the differences in composition between a stable and vulnerable plaque?

A

Stable - fibrous, more calcified, less lipid, less inflammation, less apoptosis
Vulnerable - less fibrous, less calcified, more lipid, more inflammation, more apoptosis

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22
Q

What is the distribution of atherosclerotic plaques?

A

Dorsal abdominal aorta and proximal coronary arteries -> popliteal arteries -> descending thoracic aorta -> internal carotid arteries -> renal arteries

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23
Q

2 anti-platelet drugs

A 
Aspirin
Plavix (clopidogrel)
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24
Q 
Aspirin
Plavix (clopidogrel)
A

Arginine

Nitric oxide synthase

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25
Q

What is the route of administration for heparin?

A

IV – immediate
SubQ – delayed
It is not absorbed from the gut!

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26
Q

What is the antidrug to heparin?

A

Protamine

It is a strongly + charged drug that complexes with the strongly – charged heparin

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27
Q

What are the advantages to low molecular weight heparin?

A

Longer half-life

Better bioavailability

More predictable dose response, so can be given outpatient

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28
Q

Which drug acts in the plasma to directly inhibit the activity of factor Xa?

A

Rivaroxaban

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29
Q

Which drug acts in the plasma to directly inhibit thrombin?

A

Dabigatran

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30
Q

What does streptokinase do?

A

Activates plasminogen

It’s from strep!

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31
Q

Nitric oxide synthase is expressed on the ____________ side of the endothelium

A

Luminal

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32
Q

Nitric oxide synthesis is ____________-mediated vasodilation

A

cGMP

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33
Q

What part of the heart wall is most often not perfused?

A

Subendocardium (so the inside of the wall)

Because blood vessels are on the outside

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34
Q

What are the 3 classifications of acute coronary syndrome? Draw table

A

Unstable angina - ST depression (may look normal when no pain); partial occlusion; no serum biomarkers
NSTEMI - ST depression; partial occlusion; no serum biomarkers
STEMI - ST elevation; total occlusion; serum biomarkers

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35
Q

Which vascular beds increase blood flow in exercise?

A

ONLY the muscle and coronary ones

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36
Q

What is acute coronary syndrome?

A

Atherosclerotic plaque rupture or thrombosis

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37
Q

Within what time frame do you need to be sent to the cath lab?

A

90 minutes

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38
Q

What is drug treatment protocol for unstable angina/NSTEMI?

A

2 antiplatelet agents: aspirin + P2Y12 inhibitor. If going to cath lab/high risk, consider a GP IIa/IIIb inhibitor

1 anticoagulant. If going to cath lab give bivalirudin

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39
Q

Where are the 3 natriuretic peptides found?

A

Atrial - atrium
B - ventricles
C - endothelium

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40
Q

What causes BNP levels to rise?

A

Increased stretch due to increased volume in ventricles

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41
Q

What are 3 cases in which BNP levels can be higher than expected?
What is a normal value?

A

Women
Elderly
Renal insufficiency

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42
Q

What are berry aneurysms?

A

Congenital defects in the media of arteries at the bifurcation of cerebral vessels

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43
Q

What is ischemic heart disease? What accounts for most of it?

A

Myocardial oxygen requirement > cardiac blood supply

Obstructive coronary atherosclerosis accounts for >90%

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44
Q

What are 5 causes of injury due to reperfusion?

A 
Mitochondrial dysfunction
Calcium influx -> hypercontracture
Free radical damage
Leukocyte aggregation
Platelet and complement activation
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45
Q

At what time do irreversible ultrastructural changes occur in MI?

A

1-2 hours

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46
Q

What are wavy fibers and at what time do they occur?

A

Non contractile ischemic fibers stretched with each systole

4-12 hours after MI

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47
Q

At what time point does coagulation necrosis and neutrophil infiltration occur in MI?

A

18-24 hours

24-72 hours for maximum

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48
Q

Describe gross pathology of infarcts and their time course

A

4-7 days - macrophages with disintegration of myocytes. Pallor with hyperemic border

10 days - granulation tissue. Yellow, soft with dark border

4-8 weeks - fibrosis. Firm, gray

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49
Q

Why is myocardial hypertrophy vulnerable to ischemia?

A

The capillary bed does not expand in step

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50
Q

What is the difference in structure in pathological and physiologic cardiac hypertrophy?

A

Concentric - muscles added in parallel

Muscle added in series

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51
Q

What are 3 causes of secondary hypertension?

A

Renal
Endocrine
Vascular

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52
Q

The most frequent cause of aneurysm is _________________

A

Atherosclerosis

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53
Q

Dissection is usually due to a defect in which layer of an artery?

A

Intima

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54
Q

___________ takes triglycerides out of the chylomicron into cells

A

Lipoprotein lipase

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55
Q

What does lipoprotein lipase do?

A

Takes triglycerides out of the chylomicron into cells

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56
Q

The chylomycron with much of the TG removed is ___________

A

LDL

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57
Q

What does PCSK9 do?

A

Prevents LDL receptors from going to the surface so it’s harder to clear cholesterol

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58
Q

LDL blood test equation

A

LDL = total cholesterol - HDL - (TG/5)

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59
Q

Categorize the vasculitises

A

Large vessel: Takayasu’s arteritis, termporal arteritis

Medium vessel: Vuerger’s disease, cutaneous vasculitis, Kawasaki disease, polyarteritis nodosa

Small vessel: Chur-Strauss, microscopic polyangiitis, ganulomatous with polyangiitis, cryoglobulinemia

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60
Q

What is the main difference between giant cell arteritis and Takayasu’s arteritis?

A

Takayasu’s generally affects young people from Asia and doesn’t affect the temporal artery

Giant cell arteritis mostly affects people of northern european background

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61
Q

What is an erosion type plaque?

A

Eroded/missing endothelilal layer at plaque-thrombus interface
Sparse inflammation, usually no calcification

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62
Q

What is the difference in usual cause between a transmural and subendocardial infarction?

A

Transmural - thrombus occluding a coronary artery

Subendocardial - hypoperfusion of heart

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63
Q

Are most people right or left heart dominant? What does this mean?

A

80% of people are right-heart dominant

Their posterior coronary artery comes off the RCA

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64
Q

When is the heart most vulnerable to rupture?

A

3-7 days after a transmural infarct. This is when necrosis has set in but fibrosis hasn’t yet developed

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65
Q

Where is the most common site of atherosclerotic aneurysms?

A

Lower abdominal aorta below renal arteries

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66
Q

What characterizes giant cell arteritis?

A

Granulomatous vasculitis, particularly of the temporal artery

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67
Q

How do you treat giant cell arteritis?

A

Corticosteroids

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68
Q

What characterizes polyarteritis nodosa?

A

Acute segmental necrotizing vasculitis involving small and medium sized arteries of the kidneys, GI tract, heart

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69
Q

What antibody is often present in polyarteritis nodosa?

A

P-ANCA (perinucleur antineutrophil cytoplasmic autoantibodies)

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70
Q

How do you treat polyarteritis nodosa?

A

Anti-inflammatory/immunosuppressive

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71
Q

What characterizes wegener’s granulomatosis?

What antibody is often present?

A

Idiopathic necrotizing granulomatous vasculitis of small to medium size arteries and veins (it’s a small vessel vasculitis) involving the upper and lower respiratory tracts and kidneys

C-ANCA (cytoplasmic anti neutrophilic cytoplasmic antibodies)

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72
Q

What is churg strauss syndrome?

A

Systemic vasculitis of small arteries and veins in young people with asthma and eosinophilia, mostly ivolving the lungs

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73
Q

What is granuloma pyogenicum?

A

A reactive process where polypoid granulation tissue-like nodule on skin or mucosal surfaces
In trauma or pregnancy (wher eit often regresses)

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74
Q

What is a malignant vascular tumor called?

A

Angiosarcoma

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75
Q

What test do we use to monitor heparin therapy?

A

PTT (woodpecker)

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76
Q

What test do we use to monitor warfarin therapy?

A

PT (paratrooper)

INR (intercom radio)

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77
Q

What is ecarin clotting time?

A

Derived from the venom of the saw-scaled viper

Monitor anticoagulation therpy with direct thrombin inhibitors (hirudin and dabigatran)

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78
Q

How does heparin work?

A

It binds to and accelerates the activity of antithrombin III to inhibit activated clotting factor proteases

79
Q

Which anticoagulant is safe to use in pregnancy?

A

Heparin

Warfarin is not!

80
Q

What are 4 adverse reactions to heparin?

A

Hemorrhage
Hypersensitivity
Thrombocytopenia (greater with higher molecular weight; skeet shooting)
Osteoporosis (bone tree)

81
Q

What organ does warfarin act on?

A

Liver

82
Q

Which factors does warfarin act on?

A 
C, S (sargeants)
II - beaver
7 - devil (deadly sins)
9 - cat (9 lives)
10 - fox
83
Q

What enzyme metabolizes warfarin?

A

CYP2C9 - potential effects!

84
Q

What do you give in event of a warfarin overdose?

A

Vitamin K

Prothrombin complex concentrate or fresh frozen plasma

85
Q

How does aspirin work?

A

Inhibition of COX1 and COX2, inhibiting platelet aggregation

86
Q

How does clopidogrel work?

A

ADP receptor antagonist (Aggregate Da Players), inhibiting platelet aggregation

87
Q

How does dipyridamole work?

A

Blocks phosphodiesterase breakdown of cAMP, elevating cAMP and potentiating prostacyclin’s anti-aggretory action
Pyramid tent advertising signing up for camp and sign ‘don’t PHoster Disinterest’

88
Q

What do abciximab, aptifabitide, and tirofaban do?

A

Block IIb/IIIa receptors on platelts, reducing aggregation

89
Q

What are the 3 IIb/IIIa blockers?

A

Abciximab (ABC news)
Eptifabatide (tied score)
Tirofiban (tied score)

90
Q

How do you take aspirin in an acute myocardial infarction?

A

Chewed and swallowed

91
Q

What are the 3 major determinants of myocardial oxygen consumption?

A

Contractile state
Heart rate
Myocardial wall tension

92
Q

What is the goal of chronic pharmacotherapy for angina?

What 3 drug classes are used?

A

The goal is to reduce oxygen demand with
Nitrates
Calcium channel blockers
Beta-blockers

93
Q

What is the goal of treatment of variant/Prinzmetal angina?

What 2 drug classes are used to treat?

A

Reversing/preventing vasospasm with:

Nitrates
Calcium channel blockers

94
Q

What does NO do?

A

Activates guanylate cyclase
Increases converstion og GTP to cGMP
cGMP leads to myosin light chain dephosphorylation, preventing its interaction with actin
This causes relaxation

95
Q

What are 4 side effects of therapeutic vasodilation?

A

Headache
Orthostatis hypotension
Reflex tachycardia
Facial flushing

96
Q

What are the 3 calcium channel blockers we care about?

A

Verapamil (Very vanilla)
Diltiazem (Dark chocolate)
Nifedipine (Fudge)

97
Q

Fick equation

A

CO = VO2/[a-vO2)

98
Q

The largest pressure drop in the vascular system occurs across the ______

A

Arterioles

99
Q

How do you claculate mean arterial pressure?

A

Diastolic BP + (S-D)/3

100
Q

How are flow and vessel radius related?

A

Q oc r^4

101
Q

What is the primary means of venous blood return from the lower extremities?

A

Calf muscle pump

102
Q

Which layer does atherosclerosis occur in?

A

Intima

103
Q

7 steps of atherosclerosis

A 
Fatty streak
Endothelial dysfunction
Lipoprotein entry and modification
Leukocyte recruitemnt
Foam cells
SMC migration
Plaque progression/disruption
104
Q

What makes the majority of an atherosclerotic cap’s contents?

A

SMCs

105
Q

How do statins work?

A

They are HMG-CoA inhibitors
This is the rate-limiting enzyme in cholesterol biosynthesis

Less cholesterol in cells -> LDL receptor upregulation -> cholesterol is removed from blood

106
Q

What does PSK9 do in cholesterol cycle?

A

It binds to the LDL receptor and tells it to break down

107
Q

How does the lumen size change in atherosclerosis?

A

It compensates for a while, staying the same size

Eventually as the plaque grows more, it shrinks

108
Q

What are 5 ways statins ‘stabilize’ plaques?

A

Reduce lipid content
Decrease inflammatory cells
Decrease MMP and tissue factor activation
Decrease thrombogenesis
Increased fibrosity - decreased plaque rupture

109
Q

What are the ages for premature coronary heart disease?

A

Males

110
Q

What is severe hypertriglyceridemia associated with?

A

Acute pancreatitis

111
Q

Has lowering triglycerides or raising HDL been shown to reduce death/increase health?

A

Nope! It remains unclear

112
Q

How does fractional flow reserve work?

A

Coronary catheterization to compare pressure differences in arteries. If there is a drop, there is likely a stenosis

113
Q

How long after quitting smoking does your risk of coronary events return to normal?

A

10 years

114
Q

Information regarding a patient’s INR is utilized in the management of patients who are taking __________________

A

Warfarin

115
Q

Indirect thrombin-Xa inhibitors have _______ in their names

Direct thrombin inhibitors have ________

A

parin

rudin

116
Q

In which situation would you use heparin vs. LMWH?

A

Renal impairment, since it is renally eliminated

Heparin effect is more rapidly and completely reversed by protamine

117
Q

What is the difference between what dabigatran vs. rivaroxaban inhibits?

A

Thrombin

Xa

118
Q

What is the target of warfarin?

A

Vitamin K epoxide reductase (V-KOR supply boat)

119
Q

How are dabigatran and rivaroxabaneliminated?

A

Prodrug converted by esterases; renaly excreted

Hepatic metabolism by a CYP; renally excreted

120
Q

What are 3 side effects of warfarin?

A

Necrosis of fatty soft tissues (because of increased coagulability in first doses)
GI
Osteoporosis

121
Q

What is class III data?

A

Recommendations indicate therapy should not be performed

122
Q

What class of antiplatelet drug does clopidogrel belong to?

A

P2Y12 antagonist

123
Q

How do P2Y12 receptor blockers work?

A

They block binding of ADP to a platelet receptor P2Y12
Inhibits activation of the GP IIb/IIIa complex
Inhibits platelet aggregation

124
Q

What should your blood pressure be below?

A

140/90

125
Q

How do diabetes and prior MI compare as mortality risks?

A

They confer equal mortality reisks

126
Q

What on activated endothelium (1) attaches to what on monocytes (2), allowing them to adhere?

A

VCAM-1 ataches to CD11c (integrin) and VLA-4 (tight adhesion)

127
Q

Which T cells are active in atherogenesis?

A

Th1 - promotes IFN-gammma

TH17 - plaque instability and neoangiogenesis

128
Q

What 3 things does CRP respond to?

What is its downstream effect?

A

Modified membranes
Apoptotic cells
Lipoproteins

It activates the classical complement pathway

129
Q

What is the suffix for fibrinolytic agents?

A

-teplase`

130
Q

What are the 2 main symproms of peripheral artery disease?

A

Claudication

Ischemic rest pain/ischemic ulcers/gangrene

131
Q

What ratio of the ankle-brachial index is cause for concern?

How do you calculate it?

A

.9>x>1.3

Arm BP/ankle BP

132
Q

What defines an aneurysm?

A

Increase in diameter by >50%

133
Q

4 mechanisms of aneurysm formation

A

Weakened aortic wall
Inflammation
Proteolytic enzymes
Biomechanical stresses

134
Q

2 mechanisms of aortic dissection

A

Intimal tear

Rupture of vasa vasorum

135
Q

What is Virchow’s triad?

A

Abnormal flow
Injury
Coagulation changes

136
Q

What are 3 factors that influence venous return?

A

Venoconstriction
Muscle pump
Respiratory pump - negative pressure draws blood back to heart, especially during strenuous exercize

137
Q

What is rate pressure product?

3 components of rate pressure product

A

An index of myocardial oxygen consumption

HR^2
P
V

138
Q

What are the 5 parts of the heart tube?

A 
Truncus
Bulbus cordis
Primitive ventricle
Primitive atria
Sinus venosus
139
Q

Which direction does the primitive heart loop?

A

To the right of the embryo so that the ventricles are in front, atria behind

140
Q

Which part of the heart is the pulmonary artery/aorta attached to in the embryo?

A

The right ventricle

141
Q

What is the embryologic conus?

A

The outflow tract of the ventricle

142
Q

What does the truncus become?

A

Aortic/pulmonary valves
Ascending aorta
Pulmonary trunk

143
Q

In the embryo, blood enters th eheart tube through the sinus venosus via 3 sets of veins:

A

Umbilical - from placenta
Vitelline - from yolk salk
Cardinal - drains embryo

144
Q

What are the 2 conal crests that fuse with the ventricular septum?

A

Dextrodorsal

Sinistroventral

145
Q

How do myocardial wall thickness and oxygen consumption compare?

A

They are inversely proportional

Wall stress is less,so consumption is less

146
Q

What are the 4 parts of the tetralogy of Fallot?

A
  1. RV outflow tract obstruction
  2. RV hypertrophy
  3. Dextraposition of the aorta so that the aorta overrides the ventricular septal defect
  4. Ventricular septal defect

This is all due to the anterior and superior deviation of the infundibular part of the ventricular septum

147
Q

What is a blue vs. pink tet?

A

Tetralogy of Fallot
Blue from R to L shunt if RV outflow resistance > systemic vascular resistance -> cyanosis

Pink from L to R shunt if RV outflow resistance no cyanosis

148
Q

How do you treat a tet spell (4)?

A

Knee to chest - increased systemic vascular resistance
Phenylephrine - increases SVR
Morphine - sedative
Volume expansion with IV fluids

149
Q

At what age do you repair tetralogy of Fallot?

A

2-4 months

150
Q

What disease is associated with coarctation of the aorta?

A

Turner Syndrome (15%)

151
Q

What’s an important thing on physical exam that can indicate coarctation of the aorta?

A

Absent/weak femoral pulses

152
Q

What is the 3 sign in older children and adults on cardiac X ray?

A

Aortick knob - coarctation - post-stenotic dilation looks like a 3?

Also might see rib notching - dilated intercostal arteries

153
Q

What are 3 risk factors for congenital cardiac defects?

A

Male
Maternal diabetes
Cardiac defect in a first degree relative

154
Q

What are 2 risk factors for patent ductus arteriosus?

A

Above 9000 feet elevation

Maternal rubella

155
Q

The ductus is derived from what?

A

DIstal portion of left 6th aortic arch

156
Q

What drug maintains ductal patency?

A

Prostaglandins

157
Q

What 2 drugs can close a PDA?

A

Indomethacin - protects against intraventricular hemorrhage, but decreases blood flow to kidneys/brain
Ibuprofen - prefered with renal disease

158
Q

How do the time points of atrial an ventricular septation compare?

A

THey occur at the same time

159
Q

What are the 2 causes of a secundum atrial septal defect?

A

Too large a central hole in septum primum (the osteum secundum)
Inadequate development of septum secundum

160
Q

What is a dependent shunt?

A

One hwere blood flow is dependent on pressure and resistance

161
Q

What causes the murmur in an atrial septal defect?

A

It is NOT related to blood going across the defect?

Systolic ejection murmur - excessive blood flow across pulmonary valve
Diastolic rumble - excessive blood flow across the tricuspid valve

162
Q

What happens to S2 in an atrial deptal defect?

A

A2-P2 split is more prominent b/c of higher RV pressures than normal
(split usually occurs during inspriation)

163
Q

Which way does the ventricular septum grow?

A

From apex to base (the base is where the valves are)

164
Q

What are the 4 endocardial cushions?

A

Inferior
Superior
Left
Right

165
Q

Which part of the ventricular septum is most often defective?

A

The membranous portion (the part closest to the valves)

Muscular portion is a distant second

166
Q

What defines a large ventricular defect?

What is an important feature?

A

Those that are the same diameter as the aortic orifice

These are often unrestrictive

167
Q

What is eisenmenger’s syndrome? (7)

A

Large L->R shunt
Increased pulmonary blud flow
Muscularizaiton of pulmonary arterioles (irreversible at this point)
Increased RV pressure
Shunt reversal (patient will die if hole closed at this point)
Cyanosis and clubbing
Heart/lung transplant or death

168
Q

What ae the 2 cardinal symptoms of depression? Do patients always have both?

A

Loww of interest or pleasure from important activiteis - anhedonia
Depressed mood, most of the day, nearly every day

Patients may have one or both

169
Q

How long does a depressive episode usually last in major depressive disorder?

A

6-24 months

170
Q

What is dysthymia?

A

Persistent depressive disorder

Dysthymic Eeyore

171
Q

What drug do you use for a pharmacologic stress test?

A

Dobutamine

172
Q

Statins inhibit ______

A

HMG-CoA reductase

This is the rate-limiting step in the cholesterol production pathway

173
Q

What are 5 physiologic derangements associated with depression?

A 
Autonomic dysfunction (reduced HR variability)
Elevated cortisol
Platelet activation
Endothelial dysfunction
Inflammation
174
Q

Depressed patients have elevated brain ______ turnover.

A

Serotonin

175
Q

Which part of the brain is overstimulated in depression?

A

Amygdala

176
Q

Do beta blockers cause depression?

A

No!

177
Q

3 anti-ischemic drug classes

A

Beta blockers
Nitrates
Calcium channel blockers

178
Q

4 contraindications to fibrinolytics

A

Active peptic ulcer disease
Underlying bleeding disorders
Recent stroke
Recovering from recent surgery

179
Q

What drug is used for claudication?

A

Cilostazol

180
Q

2 drug classes that reduce mortality of atherosclerosis

A

Statins

ACEI

181
Q

4 major statin benefit groups

A
  1. ASCVD
  2. High LDL
  3. Diabetes
  4. estimated 10-years ASCVD risk >=7.5%
182
Q

Can you take statins in pregnancy?

A

Nope!

183
Q

3 side effects of nitrates

A

Extensions of therapeutic vasodilation:

Headaches
Syncope/hypotension
Reflex tachycardia

184
Q

Which calcium channel bockers have effects at cardiac nodal tissue?

A

Verapamil

Diltiazem

185
Q

_________ surrounds heart tubes on day 19

A

Splanchnic mesoerm

186
Q

__________________________ lines the heart tubes

A

Endothelial cells

187
Q

Septation begins at the ___________ stage o heart looping

A

Post-loop

188
Q

_________________ becomes tihe intraventricular septum

A

Atrioventricular sulcus

189
Q

What medical therapies are available for atrial septal defect?

A

Diuretics in infants to relieve breathlessness

190
Q

Why do people squat with tetralogy of Fallot?

A

Increases systemic vascular resistance, forcing more blood to go out to the lungs

191
Q

What 4 drugs do you give for MI?

A 
Morphine
Oxygen
Nitroglycerin
Aspirin
(Mona)
192
Q

What drug class is amlodipine?

A

Calcium channel blocker

193
Q

What do nitrates do?

A

Decrease ventricular preload by dilating veins and dilating coronary arteries a little bit

Spring 2016 - CVPR (4 decks)

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